644 research outputs found
SHARED PARAMETER METHOD FOR MODELING THE EVOLUTION OF DEPRESSIVE SYMPTOMS IN LONGITUDINAL STUDIES WITH NONIGNORABLE MISSING DATA
In longitudinal studies of depressive symptoms in elderly patients, analyses are complicated by the presence of nonignorable missing data. In this study, we used data from the Monongahela Valley Independent Elders Survey (MoVIES) of 1,260 rural and elderly residents in western Pennsylvania. The method we used to analyze the evolution of depression is the shared parameter model, which is one of the methods that provide a framework for jointly modeling the longitudinal outcomes and the dropout process through a common frailty or unobserved random effects. When we used 2 different shared parameter models instead of using an unadjusted longitudinal model, we found the following decreases in the ratio of the odds of depression: a 2% decrease for women versus men (OR decreased from 2.05 in the unadjusted model to 2.00 in each shared parameter model); a 3% decrease for individuals with less than a high school education versus individuals with more than or equal to a high school education (OR decreased from 0.33 to 0.32); a 3% decrease for individuals taking fewer than 4 prescription drugs versus individuals taking 4 or more prescription drugs (OR decreased from 0.29 to 0.28); a 5% decrease for individuals using antidepressant drugs versus individuals not using antidepressant drugs (OR decreased from 16.15 to 15.35 in the first shared parameter model and to 15.39 in the second shared parameter model); and a 1% decrease for individuals with functional impairment versus individuals without functional impairment (OR decreased from 4.72 to 4.66 in the first shared parameter model and to 4.67 in the second shared parameter model). Because differences of this magnitude are likely to have an impact on decisions concerning public health policies and funding, it is important to take nonignorable missing data into account when analyzing longitudinal studies. Shared parameter models can be computationally demanding, so their performance should be judged by their goodness of fit and required running time
How do Agency Problems Affect the Implied Cost of Capital?
We test the relationship between the implied cost of capital and two agency problems, free cash flows and overinvestment. We show that free cash flows have a significant negative impact on the implied cost of capital, but overinvestment has a significantly positive impact. In addition, the pay-for-performance sensitivity has a negative effect but the sensitivity of volatility has a significantly positive effect on the implied cost of capital. After taking the incentives into account, we find that the significance of the impact from both agency problems still exists. Finally, we conclude that well-designed executive compensation should focus on reducing overinvestment and the sensitivity of volatility
Reply to "The impact of nerve sparing robotic-assisted radical prostatectomy on positive surgical margins: Uncertainty"
Effects of nerve-sparing procedures on surgical margins after robot-assisted radical prostatectomy
BACKGROUND: Nerve-sparing (NS) techniques could potentially increase positive surgical margins (PSM) after robot-assisted radical prostatectomy (RARP). Nevertheless, the available studies have revealed ambiguous results among distinct groups. This study purposed to clarify the details of NS techniques to accurately estimate their influence on margin status. METHODS: We studied RARPs performed by one surgeon from 2010 to 2018. Surgical margins were evaluated by the laterality and levels of NS techniques in site-specific prostate lobes. The multivariable analysis evaluated the effects of nerve-sparing procedures, combined with other covariate factors, on margin status. RESULTS: Overall, four hundred nineteen RARPs involving 838 prostate lobes were analyzed. Notably, 181 patients (43.4%) had pT2-stage, and 236 (56.6%) had pT3-stage cancer. The PSM rates for patients who underwent unilateral, bilateral, and non NS procedures were 30.3%, 28.8%, and 50%, respectively (p = 0.233) or in stratification by pT2 (p = 0.584) and pT3 (p = 0.116) stage. The posterolateral PSM rates among site-specific prostate lobes were 10.9%, 22.4%, and 18.9% for complete, partial, and non NS techniques, respectively (p = 0.001). The partial NS group revealed a significant increase in PSM rate compared with the complete NS (OR 2.187, 95% CI 1.19-4.03) and non NS (OR 2.237, 95% CI 1.01-4.93) groups in site-specific prostate lobes. CONCLUSION: Partial NS procedures have a potential risk of increasing the PSM rate than complete and non NS procedures do. Therefore, correct case selection is required before performing partial NS techniques
Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways
<p>Abstract</p> <p>Background</p> <p><it>H. pylori </it>infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve <it>H. pylori</it>-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.</p> <p>Results</p> <p>Challenge with <it>H. pylori </it>increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after <it>H. pylori </it>infection in a dose-dependent manner. A higher dose (MOI 100) of <it>L. acidophilus </it>pre-treatment attenuated the <it>H. pylori</it>-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. <it>L. acidophilus </it>also inhibited <it>H. pylori</it>-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. <it>L. acidophilus </it>pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting.</p> <p>Conclusions</p> <p><it>H. pylori </it>infection induces Smad7, NFκB, IL-8, and TNF-α production <it>in vitro</it>. Higher doses of <it>L. acidophilus </it>pre-treatment reduce <it>H. pylori</it>-induced inflammation through the inactivation of the Smad7 and NFκB pathways.</p
Etiology and Treatment of Childhood Peptic Ulcer Disease in Taiwan: A Single Center 9-Year Experience
Background/PurposePeptic ulcer disease (PUD) in children is relatively rare as compared with adults. This study aimed to assess the etiology, clinical and histological characteristics, and treatment of PUD in children.MethodsAll children aged < 18 years with an endoscopic diagnosis of PUD were enrolled in a tertiary referral center. The demographic data, clinical, endoscopic, and histological findings were compared between patients with different causes of PUD.ResultsFrom 1234 endoscopic examinations, 67 (5.4%) children (median age, 11.4 years) with gastric ulcer (GU; n = 27) or duodenal ulcer (DU; n = 40) were included. Thirty-two (47.7%) of them had Helicobacter pylori infection and 11 (16.5%) had previous use of non-steroidal anti-inflammatory drugs (NSAIDs). Non-H. pylori, non-NSAID PUD was found in 24 (35.8%) patients. Children with H. pylori-related PUD had a significantly higher mean age, antral chronic inflammatory score, rate of familial PUD, and presence of DU and nodular gastritis than those with NSAID-related and non-H. pylori, non-NSAID PUD (p < 0.01). In contrast, children with NSAID-related PUD had a higher rate of upper gastrointestinal bleeding, associated with acute febrile disease, than those with H. pylori-related and non-H. pylori, non-NSAID PUD (p < 0.05). All but two patients with non-H. pylori, non-NSAID PUD were disease free after H. pylori eradication and proton pump inhibitor treatment for 1–2 months.ConclusionIn children, H. pylori-related PUD is associated with familial peptic ulcer and the presence of DU. However, short-term NSAID use is correlated highly with GU. The outcome of childhood PUD is good
Unusual dyspnea in a hemodialysis patient: A case report
The typical clinical symptoms of hemothorax include a rapid development of chest pain or dyspnea, which may be life-threatening without immediate management. As we know, spontaneous hemothorax, a collection of blood within the pleural cavity without previous history of trauma or other cause, which usually onsets suddenly. The early and accurate diagnosis of spontaneous hemothorax is imperative in clinical practice. We reported a middle-age male undergoing regular hemodialysis was referred to our emergency department due to unknown cause of dyspnea and acute respiratory failure. Chest radiography revealed bilateral patchy infiltration of lung. Pleural tap analysis showed exudative pleural effusion with numerous red blood cells. Video-assisted thoracic surgery (VATS) were performed and confirmed the final diagnosis of spontaneous hemothorax. He was then successfully treated with the surgery of VATS combined chest tube thoracostomy
Different Dietary Proportions of Fish Oil Regulate Inflammatory Factors but Do Not Change Intestinal Tight Junction ZO-1 Expression in Ethanol-Fed Rats
Oxaliplatin-induced acquired long QT syndrome with torsades de pointes and myocardial injury in a patient with dilated cardiomyopathy and rectal cancer
AbstractA 67-year-old woman presented with a history of dilated cardiomyopathy with congestive heart failure since 2003, who subsequently developed lower rectal cancer (adenocarcinoma) with liver, bone, and lymph node metastasis. Abdominoperineal resection and hepatectomy were performed. The patient received two rounds of intravenous chemotherapy, including 12 and six courses of FOLFOX4 (5-fluorouracil, leucovorin, and oxaliplatin; 85 mg/m2 per cycle). She underwent a third round of intravenous FOLFOX4 because of tumor progression. During the 21st course of FOLFOX4 regimen, the patient developed ST segment depression in lead II and prolongation of QT interval with polymorphic ventricular tachycardia, torsades de pointes right after the start of oxaliplatin infusion. Immediate defibrillation and cardiopulmonary resuscitation were administered, and the patient regained spontaneous circulation and consciousness. Twelve-lead electrocardiogram showed ST segment elevation in III, aVF, and ST segment depression in V4–6 after resuscitation. To our knowledge, prolongation of QT interval with torsades de pointes and coronary spasm with myocardial injury that were stabilized in one patient following oxaliplatin infusion has not been reported. We present a patient with these rare complications
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